Maternal BDE-209 exposure during lactation causes testicular and epididymal toxicity through increased oxidative stress in peripubertal mice offspring.

Decabromodiphenyl ether (BDE-209), a flame retardant, interferes with thyroid homeostasis and androgen biosynthesis. BDE-209 evokes hyperglycemia through impaired glucose homeostasis in rat liver. This study is in continuation to our earlier work for a better understanding of whether or not BDE-209 affects testicular and epididymal physiology in relation to oxidative status in peripupertal mice offspring. Lactating female Parkes mice were orally gavaged with 500 and 700 mg/kg body weight of BDE-209 in corn oil from postnatal day (PND) 1 to PND 28. Male pups of lactating dams were sacrificed at PND 42. Maternal BDE-209 exposure during lactation increased apoptosis and oxidative status with altered expressions of various cell survival (Bcl-2), apoptotic (Bax and caspase-3) and oxidative stress (Nrf2 and HO-1) markers in testes and epididymis of peripubertal mice offspring. Testicular glucose and lactate concentrations were markedly reduced in these pups with down-regulation in GLUT3 and GLUT8 expressions and decreased LDH activity. Maternal BDE-209 exposure markedly affected fertility potential, epididymal histology, sialic acid concentration and sperm quality with decreased expression of epididymal Cx43 and AR in these mice offspring. Results thus suggest that maternal BDE-209 exposure during lactation causes reproductive toxicity in peripubertal mice offspring.